The Immunotoxicology Group is continuing studies pertaining to the role of the pulmonary immune system in the pathogenesis of lung diseases. The objectives of these studies include (1) to evaluate the potential adverse effects of inhaled agents on lung immunity - specifically lung macrophages and lung interstitial lymphocytes; (2) if possible, to examine potential mechanisms of toxicity; and (3) to relate these observed changes in immune function to clinicians and regulatory agencies so that improved treatment and monitoring may be facilitated. Studies were performed in the following areas: (1) descriptive lung immunotoxicity studies following exposure to asbestos; and (2) mechanistic studies on the role of specific cell types in the pathogenesis of asbestos related lung disease. In studies designed to elucidate the potential immunopathogenic role of pulmonary epithelial cells in the response to asbestos, the fibrogenic fibers, chrysotile and crocidolite asbestos were shown to directly stimulate a human pulmonary type-II epithelial cell line (A549) to elicit the neutrophil chemotactic cytokine interleukin-8 in the absence of other known stimuli, suggesting an important effector role for these cells in asbestos induced disease. Studies employing T-cell deficient mice to assess the role of cell mediated immunity in asbestos were concluded. These data suggest that T cells directly or indirectly influence the termination of a neutrophilic response and fibronectin release which ultimately influences the amount of collagen accumulation in the lung and are consistent with a protective role for T lymphocytes. Together, these studies point to a significant role for immune system elements in asbestos-related diseases.